Two cases of silent subcutaneous implantable cardioverter defibrillator electrode displacement.

We describe two cases of secondary prevention subcutaneous implantable cardioverter defibrillator (S-ICD) implantation and subsequent S-ICD electrode displacement which initially went undetected. One presentation was a result of a coincidental chest x-ray for respiratory exacerbation and another with an untreated episode highlighted via remote monitoring, both patients were booked to clinic for further investigation. Our findings highlighted had there been a comparison of the existing subcutaneous electrogram (S-ECG) to captured S-ECGs at time of implant the electrode displacement would have been detected beforehand. This underpins the importance of introducing the simple management strategy into routine follow-up.

Spatial and temporal relationship between focal and rotational activations and their relationship to structural remodeling in patients with persistent atrial fibrillation.

BACKGROUND: Focal and rotational activations have been demonstrated in atrial fibrillation (AF), but their relationship to each other and to structural remodeling remains unclear. OBJECTIVE: The purpose of this study was to assess the relationship of focal and rotational activations to underlying low-voltage zones (LVZs) (<0.5 mV) and to determine whether there was a temporal (≤500 ms) and spatial (≤12 mm) relationship between these activations. METHODS: Patients undergoing catheter ablation for persistent AF were included. All patients underwent pulmonary vein isolation. Unipolar signals were collected to identify focal and rotational activations using a wavefront propagation algorithm. RESULTS: In 40 patients, 105 activations were identified (57 [54.3%] focal; 48 [45.7%] rotational). Rotational activations were co-localized to LVZs (35/48 [72.9%]) whereas focal activations were not (11/57 in LVZ [19.3%]; P <.001). The proportion of the left atrium occupied by LVZs predicted rotational activations occurrence (area under the curve 0.96; 95% confidence interval 0.90-1.00; P <.001). In patients with a relatively healthy atrium, in which the atrium consisted of ≤15% LVZs, only focal activations were identified. Thirty-two of the 35 rotational activations (91.4%) located in LVZs also showed a temporal and spatial relationship to a focal activation. The presence of a LVZ within 12 mm of the focal activation was a strong predictor for whether a paired rotational activation would also occur in that vicinity. CONCLUSION: Rotational activations are largely confined to areas of structural remodeling and have a clear spatial and temporal relationship with focal activations suggesting they are dependent on them. These novel mechanistic observations outline a plausible model for patient-specific mechanisms maintaining AF.

Atrioventricular nodal ablation is an effective management strategy for atrial fibrillation in patients with hypertrophic cardiomyopathy.

BACKGROUND: Atrial fibrillation (AF) is common in patients with hypertrophic cardiomyopathy (HCM) and can be challenging to manage. Atrioventricular nodal (AVN) ablation may be an effective management strategy for AF in these patients. OBJECTIVE: The purpose of this study was to assess the efficacy of AVN ablation in HCM patients who have failed medical therapy and/or catheter ablation for AF. METHODS: A multicenter study with retrospective analysis of a prospectively collated HCM registry was performed. AVN ablation patients were identified. Baseline characteristics and device and procedural indications were collected. Symptoms defined by New York Heart Association and European Heart Rhythm Association classification and echocardiographic findings during follow-up were assessed. RESULTS: Fifty-nine patients were included in the study. Indications for AVN ablation were 6 (10.2%) inappropriate implantable cardioverter-defibrillator shock, 35 (59.3%) ineffective rate control, and 18 (30.5%) to regularize rhythm for symptom improvement. During post-AVN ablation follow-up of 79.4 ± 61.1 months, left ventricular ejection fraction (LVEF) remained stable (pre-LVEF 48.9% ± 12.6% vs post-LVEF 50.1% ± 10.1%; P = .29), even in those without a cardiac resynchronization therapy (CRT) device (pre-LVEF 54.3% ± 8.0% vs post-LVEF 53.8% ± 8.0%; P = .65). Forty-nine patients (83.1%) reported an improvement in symptoms regardless of AF type (17/21 [81.0%] paroxysmal vs 32/38 [84.2%] persistent; P = 1.00), presence of baseline left ventricular impairment (22/26 [84.6%] LVEF ≤50% vs 27/33 [81.8%] LVEF ≥50%; P = 1.00) or CRT device (27/32 [84.4%] CRT vs 22/27 [81.5%] no CRT; P = 1.00). Symptoms improved in 16 patients (89.0%) who underwent AVN ablation to regularize rhythm. CONCLUSION: AVN ablation improved symptoms without impacting left ventricular function in the majority of patients. The data suggest that AVN ablation is an effective and safe management approach for AF in HCM and should be further evaluated in larger prospective studies.

In Atrial Fibrillation, Omnipolar Voltage Maps More Accurately Delineate Scar Than Bipolar Voltage Maps.

BACKGROUND: Optimal method for voltage assessment in AF remains unclear. OBJECTIVES: This study evaluated different methods for assessing atrial voltage and their accuracy in identifying pulmonary vein reconnection sites (PVRSs) in atrial fibrillation (AF). METHODS: Patients with persistent AF undergoing ablation were included. De novo procedures: voltage assessment in AF with omnipolar voltage (OV) and bipolar voltage (BV) methodology and BV assessment in sinus rhythm (SR). Activation vector and fractionation maps were reviewed at voltage discrepancy sites on OV and BV maps in AF. AF voltage maps were compared with SR BV maps. Repeat ablation procedures: OV and BV maps in AF were compared to detect gaps in wide area circumferential ablation (WACA) lines that correlated with PVRS. RESULTS: Forty patients were included: 20 de novo and 20 repeat procedures. De novo procedure: OV vs BV maps in AF; average voltage 0.55 ± 0.18 mV vs 0.38 ± 0.12 mV; P = 0.002, voltage difference of 0.20 ± 0.07 mV; P = 0.003 at coregistered points and proportion of left atrium (LA) area occupied by low-voltage zones (LVZs) was smaller on OV maps (42.4% ± 12.8% OV vs 66.7% ± 12.7% BV; P < 0.001). LVZs identified on BV maps and not on OV maps correlated frequently to wavefront collision and fractionation sites (94.7%). OV AF maps agreed better with BV SR maps (voltage difference at coregistered points 0.09 ± 0.03 mV; P = 0.24) unlike BV AF maps (0.17 ± 0.07 mV, P = 0.002). Repeat ablation procedure: OV was superior in identifying WACA line gaps that correlated with PVRS than BV maps (area under the curve = 0.89, P < 0.001). CONCLUSIONS: OV AF maps improve voltage assessment by overcoming the impact of wavefront collision and fractionation. OV AF maps correlate better with BV maps in SR and more accurately delineate gaps on WACA lines at PVRS.

Exploiting SMART pass filter deactivation detection to minimize inappropriate subcutaneous implantable cardioverter defibrillator therapies: a real-world single-centre experience and management guide.

AIMS: The SMART Pass™ (SP) algorithm is a high-pass filter that aims to reduce inappropriate therapy (IT) in subcutaneous internal cardiac defibrillator (S-ICD), but SP can deactivate due to low amplitude sensed R waves or asystole. The association between IT and SP deactivation and management strategies were evaluated, hypothesizing SP deactivation increases the risk of IT and device re-programming, or lead/generator re-positioning could reduce this risk. METHODS AND RESULTS: Retrospective single-centre audit of Emblem™ S-ICD devices implanted 2016 to 2020 utilizing health records and remote monitoring data. Cox regression models evaluated associations between SP deactivation and IT. A total of 348 patients (27 ± 16.6 months follow-up) were studied: 73% primary prevention. Thirty-eight patients (11.8%) received 83 shocks with 27 patients (7.8%) receiving a total of 44 IT. Causes of IT were oversensing (98%) and aberrantly conducted atrial fibrillation (2%). SP deactivation occurred in 32 of 348 patients (9%) and was significantly associated with increased risk of IT (hazard ratio 5.36, 95% CI 2.37-12.13). SP deactivation was due to low amplitude R waves (94%), associated with a higher defibrillation threshold at implant and presence of arrhythmogenic right ventricular cardiomyopathy. No further IT occurred 16 ± 15.5 months after corrective interventions, with changing the sensing vector being successful in 59% of cases. CONCLUSION: To reduce the risk of IT, the cause of the SP deactivation should be investigated, and appropriate reprogramming, device, or lead modifications made. Utilizing the alert for SP deactivation and electrograms could pro-actively prevent IT.